Considering the function of KSHV in modulating angiogenesis through autocrine and paracrine mechanisms by orchestrating a multifaceted interaction involving diverse pro-angiogenic factors43,44, it may be fruitful to examine clinical KS specimens to investigate the possible pathogenic contributions of OTULIN and M1 ubiquitination to KSHV-mediated angiogenesis. The gene discussed is OTULIN; the disease is Kaposi's sarcoma.